| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2492901 | Medical Hypotheses | 2006 | 6 Pages |
SummaryIt is hypothesized that the genesis and spread of obesity is predetermined by genetic immunity to infections and subsequent interethnic genetic admixture. As in genetic immunity to infections, obesity is determined by a constitutional incongruence between relevant acting agents and their molecular targets. Because many hormones share their specific receptors with the acting molecules of infectious agents, mutant formation of a life-saving genetic resistance to infection could also create life-threatening immunity to relevant hormones. This kind of individual molecular constitution could spread in a population as a result of natural selection for genetic immunity to infections that had performed differently in ecologically distinct populations. Extraordinary diversity in the obesity course, manifestations and severity of specific affections and their sizes and focal disposition around the body, is created by the inter-ethnic mating of persons with different grades of hormone-receptor incongruence.
